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The TSH Conundrum in Thyroid Disease

Thyrotropin, which is also known as thyroid stimulating hormone or TSH, is a pituitary hormone that helps regulate thyroid hormone levels. TSH binds to the TSH receptor on thyroid cells, ordering these cells to grow and produce thyroid hormone. In the 1970s researchers understood that the pituitary gland secreted excess TSH in conditions of hypothyroidism in an effort to raise thyroid hormone levels. In hyperthyroidism, even before thyroid hormone levels rose abnormally high, the pituitary stopped secreting TSH, resulting in a low or suppressed TSH, to help prevent hyperthyroidism. Thus, finding analytical methods to measure TSH was a goal and it was met. The TSH test was intended to be used as a tool to screen people in the general population to see if they might have a thyroid disorder. The TSH was successful for this purpose for the most part (exceptions central hypothyroidism and resistance to thyroid hormone). The idea here was that once a disorder was discovered and properly diagnosed and treated, the TSH test wasn't needed as it has no real role in managing or monitoring treatment for thyroid disorders.

Patients with Graves' disease and patients with autoimmune atrophic thyroiditis, a condition of hypothyroidism, understand this problem only too well. Unfortunately, their doctors rarely do. I'm constantly asked for resources to explain how low TSH isn't a problem in a patient treated for Graves' disease and who still has a low TSH. In an effort to raise their TSH, many Graves' patients are over-medicated by physicians, causing hypothyroidism, an increase in thyroid antibody production, or even thyroid eye disease (Graves' ophthalmopathy).

TSH Suppression

In patients with TSH receptor antibodies, TSH is falsely suppressed as the gland recognizes these antibodies as if they were TSH molecules. After all, these antibodies react with the TSH receptor the same way that TSH does. Speculating that these patients have adequate TSH, the pituitary stops secreting TSH hormone in these conditions.

In 2003, J Brokken explained this quite well and it made a huge difference in some countries, particularly Sweden. See references. Unfortunately, not all physicians got the word despite several articles in Thyroid and the Journal of Clinical Endocrinology and Metabolism. In 2006, Chung et al published an article in Thyroid explaining Brokken's findings once again and theorizing that TSH receptor antibodies and the initial severity of thyrotoxicosis as well as the time for recovery in Graves' patients explained why TSH levels remain low in Graves' patients in remission after using antithyroid drug therapy. And yes, many patients fail to secrete TSH for several years after achieving remission.

In 2015 Yu and Farahai reported that post treatment hypothyroidism is common in Graves' disease either due to treatment or as a natural consequence that occurs in 20 percent of Graves' patients (due to a predominance of blocking TSH receptor antibodies). The authors describe 18 different articles reporting that in these hypothyroid patients TSH often is suppressed, something most Graves' patients have been trying to tell their doctors. Besides the effects of TSH receptor antibodies, the authors' findings include changes in pituitary thyrotroph cells that prevent the cells from producing TSH. They emphasize that continued TBII (thyroid binding and inhibiting immunoglobulins also known as total TSH receptor antibodies) positivity is associated with lower likelihood of TSH recovery.

It's no wonder that Werner and Ingbar, writing in their textbook, The Thyroid, A Fundamental and Clinical Text, 8th ed. describe thyroid patients as being euthyroid (normal thyroid function) when their FT4 levels fall within the reference range even when TSH is suppressed.